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Cardiology - hemodynamics
William Harwey (1578-1657)
• Hemodymamics
• Discovery of blood circulation and heart
function (published 1628)
• This theory was fully accepted after
discovery of pulmonary capillaries
(Marcello Malpighi - 1661).
Basic measurements on heart
Intra-ventricular
pressure
(right ventricle)
Intra-ventricular pres-
sure (left ventricle)
Venous
reservoir
Adjustable resistance
Přetlaková
komůrka
Flow indicator
Arterial resistance
ventricle
volumes
Central
venous
pressure
Heart
Flow indicator
What is right?
ventricular volume
intraventricular
pressure
filling pressure
Identical stroke volume
Bigger tension inside the wall
smaller ejection fraction
Length of sarcomere
isometric
muscle
force
Muscle length
intraventricular
pressure
Ventricular volume
isovolumic maxima stimulation by
sympaticus or
catecholamines
Heart
insufficiency
Intraventricular
pressure
Ventricular volume
isotonic maxima
Ventricular volume
Intraventricular
pressure
Isotonic contr.
Isovolumic
contraction
Diastolic work the
filling blood (made on
the heart)
Systolic work
of the heart
Intraventricular
pressure
Ventricular volume
afterload
Stroke
volume
Systolic
residual
volume
Enddiastolic
volume
preload
Intraventricular
pressure
Ventricular volume
Stroke
volume
Stroke
volume
Greater preload ...
…increases cardiac output.
Intraventricular
pressure
Ventricular volume
Stroke
volume
Stroke
volume
Smaller preload...
…decreases cardiac output.
Intraventricular
pressure
Ventricular volume
Stroke
volumje
Stroke
volume
Catecholamines
Catecholamines increase the stroke volume
…without increasing the preload !
Intraventricular
pressure
Ventricular volume
Stroke
volume
Stroke
volume
Zvýšení „afterloadu“
Bigger „afterload“ doesn’t change the stroke v.
Stroke
volume
... But increases the preload
Intraventricular
pressure
Ventricular volume
Systolický
objem
Syst.
objem
Zvýšení „afterloadu“
katecholaminy
Catecholamins ensure…
... Nor increase the preload!
that bigger „afterload“ will neither change SV
Minute cardiac output
Arterial pressure
50 torr 100 torr 150 torr 200 torr
3 l/min
4 l/min
5 l/min
6 l/min
7 l/min
increased stroke volume
Intraventricular
pressure
Ventricular volume
Stroke
volume
Stroke
volume
insufficiency
..smaller stroke volume
Stroke
volume
Increase in preload
smaller stroke volume
increased stroke volume
greater preload
Minute
cardiac
output
End-diastolic pressure
Lowering of “Starling curve”
insufficiency
greater frequency
greater preload
increased cardiac output
Intraventricular
pressure
Ventricular volume
insufficiency
smaller stroke volume
Stroke
volume
Stroke
volume
Stroke
volume
catecholamines
increased stroke volume
bigger preload
minute
cardiac
output
End-diastolic pressure
lower „Starling curve“
insufficiency
increased diastolic compliance
re-increase of „Starling curve“
catecholamines
Minute
cardiac
output
End-diastolic pressure
Heart is a pump
whose volume of the
output is governed by
its influx (i.e. pressure
on the influx)
Frank-Starling law
Symptoms of Cardiovascular
Diseases
Chest pain or discomfort
Dyspnea (abnormally uncomfortable awareness of
breathing)
Palpitations (uncomfortable awareness of beating
of the heart)
Syncope
Peripheral edema
Claudication
• Measurement and evaluation of volume and pressure provide
information about the cardiovascular system function.
• The cardiovascular system transports volume (blood) between
individual body compartments
• Blood pressure is necessary to maintain proper blood flow
• to form pressure gradient between heart and the periphery
• to overcome the peripheral resistance.
Ohm’s law
Q (flow) = P (pressure gradient) / R (resistance)
Principles in hemodynamics
evaluation
Principles in hemodynamics
evaluation
Blood volume and pressure influence heart
and vessels anatomy
–changes which are important for the
function of cardiovascular system
• heart muscle dilatation
• heart muscle hypertrophy
• Increase in vessel resistance (organ,
systemic, temporary, permanent)
Volume
Stroke (systolic) volume (SV)
• blood volume ejected from ventricle during
systole
Venous return
(Preload) myocardium
Fluid volume
venous tonus
breathing
Muscle pump
EDV ESV
SV
Vessel resistance
(Afterload)
contractility
Stroke Volume
• Depends on: preload,
afterload, contractility
• SV = EDV (enddiastolic
volume) – ESV
(endsystolic volume)
EF = SV / EDV
SV – systolic volume
EDV – endiastolic volume
Ejection fraction (EF)
Ejection fraction (EF)
• Basic parameter for evaluation of the
systolic function of the heart
• Decreased: decreased contractility (CHD,
heart failure), valvular diseases,
• Increased: hypertrofic cardiomyopathy
Normal values:
50–55 % and more
increased e.g. due to sympathetic stimulation and
other inotropic action
40 % and less in systolic dysfunction
Measurement:
most commonly by echocardiography, ev. isotope methods
Ejection fraction (EF)
EDV1
End of diastole 1
ESV1
SV1
End of systole 1
EF1 = SV1/EDV1
ESV2
SV2
EF2 = SV2/EDV2
EF2 > EF1
End of systole 2
EDV2
End of diastole 2
ESV3
SV3
EF3 = SV3/EDV3
End of systole 3
ESV1
SV1
EF1 = SV1/EDV1
EF1 > EF3
End of systole 1
SV1 = SV3
Calculate and comment EF
• Left ventricle has at the end of the diastole
volume of 145 mL. Cardiac output is 4,8
L/min. Heart rate is 90/min.
Calculate and comment EF
• EDV = 145 ml
• SV = ?
• CO = 4800 mL/min
• HR = 90/min
• SV = CO / HR = 4800 / 90 = 53,3 mL
• EF = 53,3 / 145 = 0,37 (37 %)
Calculate and comment EF
• Cardiac output is nearly normal
• Mild tachycardia
• Increased preload
• Decreased EF
Decreased effectivness of the systole is
compensated by the increase of preload
and tachycardia
Cardiac output, cardiac index
CO = HR × SV
(HR = heart rate, SV = stroke volume)
• Normal values: 4–7 L/min
CI = CO/body surface
• Normal values: 2.8 – 4.2 L/m2
Measurment:
• Thermodilution (standard) – Swan-Ganz catheter
– Fick Principle
• Noninvasive methods (Echo with Doppler)
Thermodilution method
• The applies indicator dilution principles using
temperature change as the indicator
• A known amount of solution at a known
temperature is injected rapidly into the right atrial
lumen of the catheter.
• This cooler solution mixes with and cools the
surrounding blood, and the temperature is
measured downstream in the pulmonary artery by
a thermistor embedded in the catheter.
• The resultant change in temperature is then
plotted on a time-temperature curve
Venous return
(Preload) myocardium
Fluid volume
venous tonus
breathing
Muscle pump
EDV ESV
SV
EF
Vessel resistance
(afterload) Cardiac output
Heart rate
Sympatic n.
contractility
Systolic Function of Heart
Sympatic n.
Renin-Angiotensin-Aldisteron
Pressure
Blood Pressure
• Measured in millimeters of
mercury (or kPa), within
the major arterial system of
the body
• Systolic pressure
– maximum blood pressure
during contraction of the
ventricles
• Diastolic pressure
– minimum pressure recorded
just prior to the next
contraction
Blood Pressure
• The blood pressure is
usually taken with the
patient seated using
standard blood pressure cuff
• Additional information may
be gained by checking the
patient in the lying and
standing positions
– Systolic blood pressure should
not drop more than 10 mm Hg,
and diastolic pressure should
remain unchanged or rise
slightly.
Systemic BP
• systolic: heart function
• diastolic: peripheral resistance
• mean pressure
• pressure amplitude
• hypertension, hypotension
Interpretation of Blood Pressure Measurements
in
Individuals 18 Years of Age and Older
Diastolic pressure (mm
Hg)
Category
<85 Normal
85-89 High normal
90-104 Mild hypertension
105-114 Moderate hypertension
>115 Severe hypertension
Systolic pressure (mm
Hg) (when diastolic < 90)
Category
< 140 Normal
140-159 Borderline isolated systolic hypertension
>160 Isolated systolic hypertension
Pressures in the heart
Atria
• Pressure practically depends on the pressure
in the ventricles if the valves are intact
• Pressure gradients (atrium – ventricle)
– valves open, the pressure in the atrium and
ventricle is equal in diastole
– difference originates due to valve stenosis
– the gradient reflects the tightness of stenosis
Pressures in the heart - Ventricles
(chambers)
Diastole
• during filling of the ventricles the pressure
increases, the increase depends on
compliance of the ventricle and in normal
heart the increase is only weak
Systole:
• pressure depends on heart contraction and
pressure in aorta/pulmonary artery
Invasive measurement of BP
– pressure measurements in separate heart
cavities
– wedge pressure – end-diastolic pressure
– pressure gradients
– cardiac output
– blood for oxygen saturation
– Injection of contrast dyes for angiography
– biopsy
Invasive measurement of BP
Cardiac Catheterization (A. Femoralis – AO)
Invasive measurement of BP
Cardiac Catheterization (V. cava – RA – LV – A. Pulmonaris)
Heart catheterization
• Swan-Ganz catheter position in heart
– Right atrium (RA)
– Right ventricle (RV)
– Pulmonary artery (PA)
– Pulmonary artery wedge pressure (PAWP)
Pressure tracing during catheterization
by Swan-Ganz catheter
right atrium – RA
right ventricle (RV)
pulmonary artery (PA)
PAWP
PCW
• reflect the pressure in
left atrium / ventricle (in
absence of mitral
stenosis)
• increase in
• left heart failure
• mitral stenosis
End-diastolic pressure
• the pressure in the ventricle at the end of diastole
• depends on filling (volume, preload) and
myocardial wall properties (compliance)
Normal values: 6-12 mmHg
Measurement:
• performed as (pulmonary capillary) wedge
pressure during catheterization
• P(A)WP – pulmonary (artery) wedge pressure or
PCWP – pulmonary capillary wedge pressure
Central venous pressure (CVP)
• The pressure of blood in the right atrium
• Swan-Ganz catheter or other
• Normal values: 2-8 mm Hg
• Monitoring of systemic volume filling
• CVP indirectly indicates the efficiency of the
heart's pumping action (EDP RV, if not
tricuspidal stenosis)
• Decreased due to hypovolemia,
• Increased due to hypervolemia, right heart
failure, tricuspidal stenosis
Pressure values
• pulmonary artery systolic pressure is 15 to 30
mmHg
• pulmonary artery mean pressure is 9 to 17 mmHg
(normal < 20 mmHg)
• pulmonary artery diastolic pressure is 0 to 8 mmHg
• pulmonary capillary wedge pressure is 5 to 12
mmHg (mean <12)
• right atrial pressure is 0 to 8 mmHg
Pressures in pulmonary
circulation
a. pulmonalis: 20 (30)/12/15 (20)
vv. pulmonales
lung capillaries
 7-8
left atrium 1-5 (až 12) mm Hg
right ventricle
20/1
systolic /diastolic/mean/borderline
DIASTOLE SYSTOLE
BPd atr.
BPd ventr.
BPs atr.
BPs ventr.
BPd atrium =BPd ventricle
Pressures in atrium and
ventricle
DIASTOLE SYSTOLE
BPd atr.
BPd ventr.
BPs atr.
BPs ventr.
STENOSIS REGURGITATION
BPd atrium >BPd ventricle
aorta
LK
LS
equal pressure
ventricle-aorta
in systole
equal pressure
ventricle-atrium
in diastole
SYSTOLE DIASTOLE
Pressures in heart valve
diseases
Mitral stenosis
• Simultaneous recording of pressures
in the pulmonary artery wedge
position (PAW) and the left ventricle
(LV)
• large gradient in diastole across the
mitral valve. The PAW pressure is
markedly elevated.
• Increased pressure in LA improves
diastolic flow to LV, LA
hypertrophies etc.
• Increased PAW may lead to
pulmonary edema
Pressures in heart valve
diseases
Mitral regurgitation
• increase of pressure in LA
during ventricle contraction
(part of the blood returns to the
atrium)
LA dilation and hypertrophy
• due to stenosis the pressure in LV
increases and becomes higher than
pressure in aorta (Ao)
• pressure gradient results
(normally both pressure peaks equal)
• important hypertrophy of LV
Pressures in heart valve
diseases
Aortic stenosis
Pressures in heart valve
diseases
Aortic regurgitation
• due to backward flow the aortic
pressure declines more rapidly
• to compensate (to maintain
normal mean pressure)
systolic pressure increases
• increased pressure amplitude
Case Study – KVS1
• M 23 yr., admitted to the hospital for
malignant hypertension.
• DM from 8 yr. of age fail to take insulin and
diet
• fail to take anti-hypertension medication
• 1 wk. before the admission was tired,
blurred vision, vomiting.
• 12 h before the admission speech failure
• BP 220/140, No orthostatic
• Edema of lower extremities
Case Study – KVS1
Ophthalmologic evaluation: bilateral edema
of papilla with hemorrhages and exudates,
arterial vasoconstriction.
Note the hard exudates in white, the hemorrhages in red, and the blurred disk margin.
This is grade four hypertensive retinopathy.
Hypertensive retinopathy (grade IV)
Case Study – KVS1
Laboratory
• - hyperkaliemia
• - low bicarbonates
• - creatinin 20.3 mg/dl (high)
• - proteinuria
• - hematuria (40-50 RBC per high power
field.)
Case Study – KVS1
Chest X-ray: enlarged heart -
cardiomegaly
Case Study – KVS1
ECG: hypertrophy of LV
EKG: Deep QRS waves on anterior chest leads which illustrate left
ventricular hypertrophy Case Study – KVS1
• Diagnosis:
– hypertension crisis
– kidney failure
– Target Organ Dammage (Heart hypertrophy,
kidney failure, Retinopathy, Cerebrovascular
disease)
• Th:
– I.V. nitroprusside
– hemodialisis (kidney transplantation)
Case Study – KVS1
• Ultrasound – Echo
• Chest X-ray
• Angiography - Coronarography
• MRI – Magnetic resonance imaging
• CT – computer tomography
• PET (positrone emission tomography –
evaluation of heart metabolism
• Radioisotope methods
Imaging methods
Ultrasound – Echo
Aortální insuficience (regurgitace) Mitrální insuficience (regurgitace)
Ultrasound – Echo
Thrombus in Left
Ventricle
(Echocardigrafy)
occupies a substantial
portion of the LV apex
Chest X-ray
Coronarography
Coronarography
Ventriculography
MRI
CT
• Perfusion Thallium scan (Tl201)
• Thallium: enters intracellular compartments,
kinetics comparable to Potassium
• Diagnosis of ischemia
• Isotope ventriculography
Radioisotope imaging
methods
Biochemical markers for acute
myocardial infarction
Laboratory tests
Diagnosis of acute myocardial infarction:
(necrotic tissue and the reaction of the organismu)
-CK-MB,
-AST,
-LD,
-myoglobin,
-troponins,
-leucocytes,
-FW
BNP (brain natriuretic peptide) in heart failure
Fick principle
To measure oxygen consumption or cardiac output (CO)
blood flow in the lung
consumption O2 = --------------------------------------------
arterial O2 - venous O2
consumption of O2
CO = ---------------------------------------------------
AV difference
Example:
1 L of arter. blood contains cca 200 mL of oxygen, 1 L of mixed ven. blood 150 mL.
AV difference is thus 50 mL/L of blood. These values can be determined by
catheterization and oxygen measurment.
Oxygen consumption in 1 min is 250 mL (measurement of estimation,
e.g. 3 mL O2/min/kg or 125 mL/min/m2).
CO is in this case 250/50, i.e. 5 L per minute.
VO2 = VE × (FiO2 - FeO2)
VE – minutová ventilace
Fi – inspirační frakce
Fe – exspirační frakce
Bude-li SV nízký – zhoršená perfuze orgánů
-únava
-slabost
-nízké prokrvení ledvin --- aktivace systému RAA
ALDOSTERON
retence Na+
ANGIOTENZIN II
vazokonstrikce
snížení GF
mitogenní účinky na srd. sval
Pathophysiology of Cardiovascular
system
• Hypertension
• Ischemia
• Arhythmia
• Diseases of endo-, myo-, peri-cardium
• Valve diseases and inherited cardiac defects

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3-cardiology-hemodynamics.ppt

  • 2. William Harwey (1578-1657) • Hemodymamics • Discovery of blood circulation and heart function (published 1628) • This theory was fully accepted after discovery of pulmonary capillaries (Marcello Malpighi - 1661).
  • 3. Basic measurements on heart Intra-ventricular pressure (right ventricle) Intra-ventricular pres- sure (left ventricle) Venous reservoir Adjustable resistance Přetlaková komůrka Flow indicator Arterial resistance ventricle volumes Central venous pressure Heart Flow indicator
  • 6. Identical stroke volume Bigger tension inside the wall smaller ejection fraction
  • 8. intraventricular pressure Ventricular volume isovolumic maxima stimulation by sympaticus or catecholamines Heart insufficiency
  • 11. Diastolic work the filling blood (made on the heart) Systolic work of the heart Intraventricular pressure Ventricular volume afterload Stroke volume Systolic residual volume Enddiastolic volume preload
  • 15. Intraventricular pressure Ventricular volume Stroke volume Stroke volume Zvýšení „afterloadu“ Bigger „afterload“ doesn’t change the stroke v. Stroke volume ... But increases the preload
  • 16. Intraventricular pressure Ventricular volume Systolický objem Syst. objem Zvýšení „afterloadu“ katecholaminy Catecholamins ensure… ... Nor increase the preload! that bigger „afterload“ will neither change SV
  • 17. Minute cardiac output Arterial pressure 50 torr 100 torr 150 torr 200 torr 3 l/min 4 l/min 5 l/min 6 l/min 7 l/min
  • 18. increased stroke volume Intraventricular pressure Ventricular volume Stroke volume Stroke volume insufficiency ..smaller stroke volume Stroke volume Increase in preload
  • 19. smaller stroke volume increased stroke volume greater preload Minute cardiac output End-diastolic pressure Lowering of “Starling curve” insufficiency
  • 20. greater frequency greater preload increased cardiac output Intraventricular pressure Ventricular volume insufficiency smaller stroke volume Stroke volume Stroke volume Stroke volume catecholamines
  • 21. increased stroke volume bigger preload minute cardiac output End-diastolic pressure lower „Starling curve“ insufficiency increased diastolic compliance re-increase of „Starling curve“ catecholamines
  • 22. Minute cardiac output End-diastolic pressure Heart is a pump whose volume of the output is governed by its influx (i.e. pressure on the influx) Frank-Starling law
  • 23. Symptoms of Cardiovascular Diseases Chest pain or discomfort Dyspnea (abnormally uncomfortable awareness of breathing) Palpitations (uncomfortable awareness of beating of the heart) Syncope Peripheral edema Claudication
  • 24.
  • 25. • Measurement and evaluation of volume and pressure provide information about the cardiovascular system function. • The cardiovascular system transports volume (blood) between individual body compartments • Blood pressure is necessary to maintain proper blood flow • to form pressure gradient between heart and the periphery • to overcome the peripheral resistance. Ohm’s law Q (flow) = P (pressure gradient) / R (resistance) Principles in hemodynamics evaluation
  • 26. Principles in hemodynamics evaluation Blood volume and pressure influence heart and vessels anatomy –changes which are important for the function of cardiovascular system • heart muscle dilatation • heart muscle hypertrophy • Increase in vessel resistance (organ, systemic, temporary, permanent)
  • 28. Stroke (systolic) volume (SV) • blood volume ejected from ventricle during systole
  • 29. Venous return (Preload) myocardium Fluid volume venous tonus breathing Muscle pump EDV ESV SV Vessel resistance (Afterload) contractility Stroke Volume • Depends on: preload, afterload, contractility • SV = EDV (enddiastolic volume) – ESV (endsystolic volume)
  • 30. EF = SV / EDV SV – systolic volume EDV – endiastolic volume Ejection fraction (EF)
  • 31. Ejection fraction (EF) • Basic parameter for evaluation of the systolic function of the heart • Decreased: decreased contractility (CHD, heart failure), valvular diseases, • Increased: hypertrofic cardiomyopathy
  • 32. Normal values: 50–55 % and more increased e.g. due to sympathetic stimulation and other inotropic action 40 % and less in systolic dysfunction Measurement: most commonly by echocardiography, ev. isotope methods Ejection fraction (EF)
  • 34. ESV1 SV1 End of systole 1 EF1 = SV1/EDV1
  • 35. ESV2 SV2 EF2 = SV2/EDV2 EF2 > EF1 End of systole 2
  • 38. ESV1 SV1 EF1 = SV1/EDV1 EF1 > EF3 End of systole 1 SV1 = SV3
  • 39. Calculate and comment EF • Left ventricle has at the end of the diastole volume of 145 mL. Cardiac output is 4,8 L/min. Heart rate is 90/min.
  • 40. Calculate and comment EF • EDV = 145 ml • SV = ? • CO = 4800 mL/min • HR = 90/min • SV = CO / HR = 4800 / 90 = 53,3 mL • EF = 53,3 / 145 = 0,37 (37 %)
  • 41. Calculate and comment EF • Cardiac output is nearly normal • Mild tachycardia • Increased preload • Decreased EF Decreased effectivness of the systole is compensated by the increase of preload and tachycardia
  • 42. Cardiac output, cardiac index CO = HR × SV (HR = heart rate, SV = stroke volume) • Normal values: 4–7 L/min CI = CO/body surface • Normal values: 2.8 – 4.2 L/m2 Measurment: • Thermodilution (standard) – Swan-Ganz catheter – Fick Principle • Noninvasive methods (Echo with Doppler)
  • 43. Thermodilution method • The applies indicator dilution principles using temperature change as the indicator • A known amount of solution at a known temperature is injected rapidly into the right atrial lumen of the catheter. • This cooler solution mixes with and cools the surrounding blood, and the temperature is measured downstream in the pulmonary artery by a thermistor embedded in the catheter. • The resultant change in temperature is then plotted on a time-temperature curve
  • 44. Venous return (Preload) myocardium Fluid volume venous tonus breathing Muscle pump EDV ESV SV EF Vessel resistance (afterload) Cardiac output Heart rate Sympatic n. contractility Systolic Function of Heart Sympatic n. Renin-Angiotensin-Aldisteron
  • 46. Blood Pressure • Measured in millimeters of mercury (or kPa), within the major arterial system of the body • Systolic pressure – maximum blood pressure during contraction of the ventricles • Diastolic pressure – minimum pressure recorded just prior to the next contraction
  • 47. Blood Pressure • The blood pressure is usually taken with the patient seated using standard blood pressure cuff • Additional information may be gained by checking the patient in the lying and standing positions – Systolic blood pressure should not drop more than 10 mm Hg, and diastolic pressure should remain unchanged or rise slightly.
  • 48. Systemic BP • systolic: heart function • diastolic: peripheral resistance • mean pressure • pressure amplitude • hypertension, hypotension
  • 49. Interpretation of Blood Pressure Measurements in Individuals 18 Years of Age and Older Diastolic pressure (mm Hg) Category <85 Normal 85-89 High normal 90-104 Mild hypertension 105-114 Moderate hypertension >115 Severe hypertension Systolic pressure (mm Hg) (when diastolic < 90) Category < 140 Normal 140-159 Borderline isolated systolic hypertension >160 Isolated systolic hypertension
  • 50. Pressures in the heart Atria • Pressure practically depends on the pressure in the ventricles if the valves are intact • Pressure gradients (atrium – ventricle) – valves open, the pressure in the atrium and ventricle is equal in diastole – difference originates due to valve stenosis – the gradient reflects the tightness of stenosis
  • 51. Pressures in the heart - Ventricles (chambers) Diastole • during filling of the ventricles the pressure increases, the increase depends on compliance of the ventricle and in normal heart the increase is only weak Systole: • pressure depends on heart contraction and pressure in aorta/pulmonary artery
  • 52. Invasive measurement of BP – pressure measurements in separate heart cavities – wedge pressure – end-diastolic pressure – pressure gradients – cardiac output – blood for oxygen saturation – Injection of contrast dyes for angiography – biopsy
  • 53. Invasive measurement of BP Cardiac Catheterization (A. Femoralis – AO)
  • 54. Invasive measurement of BP Cardiac Catheterization (V. cava – RA – LV – A. Pulmonaris)
  • 55. Heart catheterization • Swan-Ganz catheter position in heart – Right atrium (RA) – Right ventricle (RV) – Pulmonary artery (PA) – Pulmonary artery wedge pressure (PAWP)
  • 56. Pressure tracing during catheterization by Swan-Ganz catheter right atrium – RA right ventricle (RV) pulmonary artery (PA) PAWP PCW • reflect the pressure in left atrium / ventricle (in absence of mitral stenosis) • increase in • left heart failure • mitral stenosis
  • 57. End-diastolic pressure • the pressure in the ventricle at the end of diastole • depends on filling (volume, preload) and myocardial wall properties (compliance) Normal values: 6-12 mmHg Measurement: • performed as (pulmonary capillary) wedge pressure during catheterization • P(A)WP – pulmonary (artery) wedge pressure or PCWP – pulmonary capillary wedge pressure
  • 58. Central venous pressure (CVP) • The pressure of blood in the right atrium • Swan-Ganz catheter or other • Normal values: 2-8 mm Hg • Monitoring of systemic volume filling • CVP indirectly indicates the efficiency of the heart's pumping action (EDP RV, if not tricuspidal stenosis) • Decreased due to hypovolemia, • Increased due to hypervolemia, right heart failure, tricuspidal stenosis
  • 59. Pressure values • pulmonary artery systolic pressure is 15 to 30 mmHg • pulmonary artery mean pressure is 9 to 17 mmHg (normal < 20 mmHg) • pulmonary artery diastolic pressure is 0 to 8 mmHg • pulmonary capillary wedge pressure is 5 to 12 mmHg (mean <12) • right atrial pressure is 0 to 8 mmHg
  • 60. Pressures in pulmonary circulation a. pulmonalis: 20 (30)/12/15 (20) vv. pulmonales lung capillaries  7-8 left atrium 1-5 (až 12) mm Hg right ventricle 20/1 systolic /diastolic/mean/borderline
  • 61. DIASTOLE SYSTOLE BPd atr. BPd ventr. BPs atr. BPs ventr. BPd atrium =BPd ventricle Pressures in atrium and ventricle
  • 62. DIASTOLE SYSTOLE BPd atr. BPd ventr. BPs atr. BPs ventr. STENOSIS REGURGITATION BPd atrium >BPd ventricle
  • 63. aorta LK LS equal pressure ventricle-aorta in systole equal pressure ventricle-atrium in diastole SYSTOLE DIASTOLE
  • 64. Pressures in heart valve diseases Mitral stenosis • Simultaneous recording of pressures in the pulmonary artery wedge position (PAW) and the left ventricle (LV) • large gradient in diastole across the mitral valve. The PAW pressure is markedly elevated. • Increased pressure in LA improves diastolic flow to LV, LA hypertrophies etc. • Increased PAW may lead to pulmonary edema
  • 65. Pressures in heart valve diseases Mitral regurgitation • increase of pressure in LA during ventricle contraction (part of the blood returns to the atrium) LA dilation and hypertrophy
  • 66. • due to stenosis the pressure in LV increases and becomes higher than pressure in aorta (Ao) • pressure gradient results (normally both pressure peaks equal) • important hypertrophy of LV Pressures in heart valve diseases Aortic stenosis
  • 67. Pressures in heart valve diseases Aortic regurgitation • due to backward flow the aortic pressure declines more rapidly • to compensate (to maintain normal mean pressure) systolic pressure increases • increased pressure amplitude
  • 68. Case Study – KVS1 • M 23 yr., admitted to the hospital for malignant hypertension. • DM from 8 yr. of age fail to take insulin and diet • fail to take anti-hypertension medication • 1 wk. before the admission was tired, blurred vision, vomiting. • 12 h before the admission speech failure • BP 220/140, No orthostatic • Edema of lower extremities Case Study – KVS1
  • 69. Ophthalmologic evaluation: bilateral edema of papilla with hemorrhages and exudates, arterial vasoconstriction. Note the hard exudates in white, the hemorrhages in red, and the blurred disk margin. This is grade four hypertensive retinopathy. Hypertensive retinopathy (grade IV) Case Study – KVS1
  • 70. Laboratory • - hyperkaliemia • - low bicarbonates • - creatinin 20.3 mg/dl (high) • - proteinuria • - hematuria (40-50 RBC per high power field.) Case Study – KVS1
  • 71. Chest X-ray: enlarged heart - cardiomegaly Case Study – KVS1
  • 72. ECG: hypertrophy of LV EKG: Deep QRS waves on anterior chest leads which illustrate left ventricular hypertrophy Case Study – KVS1
  • 73. • Diagnosis: – hypertension crisis – kidney failure – Target Organ Dammage (Heart hypertrophy, kidney failure, Retinopathy, Cerebrovascular disease) • Th: – I.V. nitroprusside – hemodialisis (kidney transplantation) Case Study – KVS1
  • 74. • Ultrasound – Echo • Chest X-ray • Angiography - Coronarography • MRI – Magnetic resonance imaging • CT – computer tomography • PET (positrone emission tomography – evaluation of heart metabolism • Radioisotope methods Imaging methods
  • 76. Aortální insuficience (regurgitace) Mitrální insuficience (regurgitace) Ultrasound – Echo
  • 77. Thrombus in Left Ventricle (Echocardigrafy) occupies a substantial portion of the LV apex
  • 82. MRI
  • 83. CT
  • 84. • Perfusion Thallium scan (Tl201) • Thallium: enters intracellular compartments, kinetics comparable to Potassium • Diagnosis of ischemia • Isotope ventriculography Radioisotope imaging methods
  • 85. Biochemical markers for acute myocardial infarction
  • 86. Laboratory tests Diagnosis of acute myocardial infarction: (necrotic tissue and the reaction of the organismu) -CK-MB, -AST, -LD, -myoglobin, -troponins, -leucocytes, -FW BNP (brain natriuretic peptide) in heart failure
  • 87. Fick principle To measure oxygen consumption or cardiac output (CO) blood flow in the lung consumption O2 = -------------------------------------------- arterial O2 - venous O2 consumption of O2 CO = --------------------------------------------------- AV difference Example: 1 L of arter. blood contains cca 200 mL of oxygen, 1 L of mixed ven. blood 150 mL. AV difference is thus 50 mL/L of blood. These values can be determined by catheterization and oxygen measurment. Oxygen consumption in 1 min is 250 mL (measurement of estimation, e.g. 3 mL O2/min/kg or 125 mL/min/m2). CO is in this case 250/50, i.e. 5 L per minute.
  • 88. VO2 = VE × (FiO2 - FeO2) VE – minutová ventilace Fi – inspirační frakce Fe – exspirační frakce
  • 89. Bude-li SV nízký – zhoršená perfuze orgánů -únava -slabost -nízké prokrvení ledvin --- aktivace systému RAA ALDOSTERON retence Na+ ANGIOTENZIN II vazokonstrikce snížení GF mitogenní účinky na srd. sval
  • 90. Pathophysiology of Cardiovascular system • Hypertension • Ischemia • Arhythmia • Diseases of endo-, myo-, peri-cardium • Valve diseases and inherited cardiac defects